Long-term calcitonin therapy in postmenopausal osteoporosis

Gruber, Helen E.; Ivey, Joel L.; Baylink, David J.; Matthews, Meredith; Nelp, Wil B.; Sisom, Karen; Chesnut, Charles H.

doi:10.1016/0026-0495(84)90187-2

Cited by 319 publications

(95 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A decrease in ovarian estrogen production is the predominant cause of rapid bone loss during the first decade after menopause. 1,2) Osteoporosisis a serious public health problem worldwide, and is a major contributor to the high frequency of bone fracture in elderly women. The most effective approach to preventing postmenopausal osteoporosis is hormone replacement therapy such as estragiol, 3) but this therapy increases the risk of breast and uterine cancers.…”

Section: Improvement Of Bone Strength and Dermal Thickness Due To Diementioning

confidence: 99%

Improvement of Bone Strength and Dermal Thickness Due to Dietary Edible Bird’s Nest Extract in Ovariectomized Rats

Matsukawa

Matsumoto

Bukawa³

et al. 2011

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

Section: Improvement Of Bone Strength and Dermal Thickness Due To Diementioning

confidence: 99%

Improvement of Bone Strength and Dermal Thickness Due to Dietary Edible Bird’s Nest Extract in Ovariectomized Rats

Matsukawa

Matsumoto

Bukawa³

et al. 2011

Bioscience, Biotechnology, and Biochemistry

View full text Add to dashboard Cite

“…menstrual cycle * menarche * menopause Postmenopausal bone mineral density is dependent on both the amount ofbone mass accumulated during infancy and adolescence and the rate of bone loss that occurs with menopause and aging (1). Since pharmacological interventions currently in vogue for the treatment of established osteoporotic syndromes can only maintain bone mass, or at best achieve modest transient increases (2)(3)(4), prevention ofbone loss with early intervention currently appears to be the best strategy for the management of osteoporosis. In fact, osteoporosis prevention programs could be directed not only to reduce the rapid bone loss that follows menopause but also to potentiate the accumulation of bone mass during infancy through early adulthood.…”

Section: Introductionmentioning

confidence: 99%

Estrogen status and heredity are major determinants of premenopausal bone mass.

Armamento-Villareal¹,

Villareal²,

Avioli³

et al. 1992

J. Clin. Invest.

126

View full text Add to dashboard Cite

IntroductionTo analyze their relative effects on premenopausal bone mass, we have studied the impact of lifelong estrogen exposure, assessed by an estrogen score (ES; computed on age at menarche, average length of menstrual cycles since menarche, and use of birth control pills), heredity, and some environmental factors on vertebral bone density (VBD), of 63 premenopausal women (age, 19-40 yr). Compared with women with normal bone density (Z score > -1), subjects with low VBD (Z score < - Postmenopausal bone mineral density is dependent on both the amount ofbone mass accumulated during infancy and adolescence and the rate of bone loss that occurs with menopause and aging (1). Since pharmacological interventions currently in vogue for the treatment of established osteoporotic syndromes can only maintain bone mass, or at best achieve modest transient increases (2-4), prevention ofbone loss with early intervention currently appears to be the best strategy for the management of osteoporosis. In fact, osteoporosis prevention programs could be directed not only to reduce the rapid bone loss that follows menopause but also to potentiate the accumulation of bone mass during infancy through early adulthood. Ideally, the achievement of an adequate peak bone mass at skeletal maturity should constitute the best protection against potential future bone loss. Hence, the identification of factors that influence the development of optimal bone density are of utmost importance, since this information may aid researchers and clinicians to devise the most appropriate strategies for maximizing bone mass in the developmental period. Both genetic and environmental factors have been invoked as determinants ofpeak bone mass (5-8, 11, 14, 15, 32, 37). A relevant role of heredity has been recently underscored by observations of reduced bone densities in daughters of women with osteoporosis compared with those of normal mothers (6) and from twin studies showing greater concordance in bone densities between monozygotic than dizygotic twins (7,8). Since this concordance decreases as the twin pairs age, it appears that factors related to the environment play an increasingly important role as aging ensues. Postmenopausal bone loss is clearly related to estrogen deficiency (9) and can be prevented by estrogen replacement (3)

show abstract

“…A sharp decrease in estrogen production causes rapid hormone-related bone loss during the first decade after menopause. 3) Post-menopausal estrogen replacement therapy (ERT) has shown potential for reduction or prevention of coronary heart disease, 4) and is considered to be the most effective method to reduce the rate of osteoporosis in post menopausal women. 5) However, ERT may be accompanied by unacceptable side effects such as endometrial and breast cancer in some women.…”

mentioning

confidence: 99%

Comparative Study on Reduction of Bone Loss and Lipid Metabolism Abnormality in Ovariectomized Rats by Soy Isoflavones, Daidzin, Genistin, and Glycitin.

Uesugi¹,

Toda²,

Tsuji

et al. 2001

Biological & Pharmaceutical Bulletin

111

View full text Add to dashboard Cite

The risk of coronary heart disease drastically increases after menopause. 1) Arteriolosclerosis induced by lipid metabolism abnormality after menopause has been recognized as a major risk factor for cardiovascular disease.2) Osteoporosis associated with ovarian hormone deficiency following menopause is the most common cause of age-related bone loss. A sharp decrease in estrogen production causes rapid hormone-related bone loss during the first decade after menopause. 3)Post-menopausal estrogen replacement therapy (ERT) has shown potential for reduction or prevention of coronary heart disease, 4) and is considered to be the most effective method to reduce the rate of osteoporosis in post menopausal women.5) However, ERT may be accompanied by unacceptable side effects such as endometrial and breast cancer in some women. 6) Therefore, ERT is recommended only for women who have no contraindications. Thus, it would be most helpful to discover a natural and safe dietary substance that minimizes bone loss and/or improves lipid metabolism in post menopausal women.It is well known that soybeans contain free isoflavones, daidzein, genistein and glycitein, and their glycoside derivatives. Daidzin, genistin and their acylated derivatives account for the major portion of isoflavones in soybeans, while glycitin and its acylated derivatives are minor components.7) It is not easy to prepare gram amounts of isoflavones, especially glycitein and glycitin, from soybeans or by synthesis for biological testing in vivo. 7,8) Both in vitro and in vivo studies have shown that daidzein, genistein, and their glycosides exert a weak estrogenic effect. 9) Therefore, numerous studies have been performed with daidzein and genistein, but there has been only one biological study on the estrogenic activity of glycitein in vitro and in vivo, 10) to our knowledge. Several investigators have reported that soybean consumption may contribute to lower risk of the postmenopausal diseases, including coronary heart disease 11) and osteoporosis. 12)Recently, the hypocholesterolemic and osteoporosis-ameliorating properties of soy protein isolate, which is a rich source of isoflavones, have received much attention.13) It is not yet clear whether the preventive effect of soy protein on lipid and bone metabolism abnormality is due to its amino acid composition, to nonprotein constituents such as saponins, phytic acids and isoflavones, or to a combination of these factors. However, there has been increasing interest in the soy isoflavones and their biological activities in recent year. 14)Several recent reports indicate that soy isoflavones may have beneficial effects on bone. Recent studies indicate that oral administration of daidzin, genistin and their succinyl derivatives significantly prevents bone loss in an ovx model 15) and genistein is also effective.16) Further, daidzin inhibits atrophy of the uterus, while genistin or genistein does not at the examined dose. The findings of these studies suggest that the action mechanism of daidzin on bone loss is ...

show abstract

Long-term calcitonin therapy in postmenopausal osteoporosis

Cited by 319 publications

References 24 publications

Improvement of Bone Strength and Dermal Thickness Due to Dietary Edible Bird’s Nest Extract in Ovariectomized Rats

Improvement of Bone Strength and Dermal Thickness Due to Dietary Edible Bird’s Nest Extract in Ovariectomized Rats

Estrogen status and heredity are major determinants of premenopausal bone mass.

Comparative Study on Reduction of Bone Loss and Lipid Metabolism Abnormality in Ovariectomized Rats by Soy Isoflavones, Daidzin, Genistin, and Glycitin.

Contact Info

Product

Resources

About